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Particulate matters increase epithelial-mesenchymal transition and lung fibrosis through the ETS-1/NF-κB-dependent pathway in lung epithelial cells

Authors
  • Chen, Yu-Chen1
  • Chuang, Tzu-Yi2, 3
  • Liu, Chen-Wei4
  • Liu, Chi-Wei5
  • Lee, Tzu-Lin1
  • Lai, Tsai-Chun1
  • Chen, Yuh-Lien1
  • 1 College of Medicine, National Taiwan University, No. 1, Sec 1, Jen-Ai Road, Taipei, Taiwan, Republic of China , Taipei (Taiwan)
  • 2 Min-Sheng General Hospital, No. 168 Ching-Kuo Road, Taoyuan, Taiwan, Republic of China , Taoyuan (Taiwan)
  • 3 College of Medicine and National Taiwan University Hospital, No.7, Chung-Shan South Road, Taipei, Taiwan, Republic of China , Taipei (Taiwan)
  • 4 University of Arizona College of Medicine, Phoenix, AZ, USA , Phoenix (United States)
  • 5 Taoyuan General Hospital, Ministry of Health and Welfare, Taoyuan, Taiwan, Republic of China , Taoyuan (Taiwan)
Type
Published Article
Journal
Particle and Fibre Toxicology
Publisher
BioMed Central
Publication Date
Aug 14, 2020
Volume
17
Issue
1
Identifiers
DOI: 10.1186/s12989-020-00373-z
Source
Springer Nature
Keywords
License
Green

Abstract

BackgroundParticulate matters (PMs) in ambient air pollution are closely related to the incidence of respiratory diseases and decreased lung function. Our previous report demonstrated that PMs-induced oxidative stress increased the expression of proinflammatory intracellular adhesion molecule-1 (ICAM-1) through the IL-6/AKT/STAT3/NF-κB pathway in A549 cells. However, the role of O-PMs in epithelial-mesenchymal transition (EMT) development and pulmonary fibrosis and the related mechanisms have not been determined. The aim of this study was to investigate the effects of O-PMs on the pathogenesis of EMT and pulmonary fibrosis as well as the expression of ETS-1 and NF-κB p65, in vitro and in vivo.ResultsO-PMs treatment induced EMT development, fibronectin expression, and cell migration. O-PMs affected the expression of the EMT-related transcription factors NF-κB p65 and ETS-1. Interference with NF-κB p65 significantly decreased O-PMs-induced fibronectin expression. In addition, O-PMs affected the expression of fibronectin, E-cadherin, and vimentin through modulating ETS-1 expression. ATN-161, an antagonist of integrin α5β1, decreased the expression of fibronectin and ETS-1 and EMT development. EMT development and the expression of fibronectin and ETS-1 were increased in the lung tissue of mice after exposure to PMs for 7 and 14 days. There was a significant correlation between fibronectin and ETS-1 expression in human pulmonary fibrosis tissue.ConclusionO-PMs can induce EMT and fibronectin expression through the activation of transcription factors ETS-1 and NF-κB in A549 cells. PMs can induce EMT development and the expression of fibronectin and ETS-1 in mouse lung tissues. These findings suggest that the ETS-1 pathway could be a novel and alternative mechanism for EMT development and pulmonary fibrosis.

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